CCL20 in psoriasis: A potential biomarker of disease severity, inflammation, and impaired vascular health - 10/03/21
Abstract |
Background |
Psoriasis is associated with increased cardiovascular risk that is not captured by traditional proinflammatory biomarkers.
Objective |
To investigate the relationship between Psoriasis Area and Severity Index, circulating proinflammatory biomarkers, and vascular health in psoriasis.
Methods |
In patients with psoriasis and in age and sex-matched controls, 273 proteins were analyzed with the Proseek Multiplex Cardiovascular disease reagents kit and Inflammatory reagents kit (Olink Bioscience), whereas vascular endothelial inflammation and health were measured via direct transcriptomic analysis of brachial vein endothelial cells.
Results |
In psoriasis, chemokine ligand 20 (CCL20), interleukin (IL) 6, and IL-17A were the top 3 circulating proinflammatory cytokines. Vascular endothelial inflammation correlated with CCL20 (r = 0.55; P < .001) and less so with IL-6 (r = 0.36; P = .04) and IL-17A (r = 0.29; P = .12). After adjustment for potential confounders, the association between CCL20 and vascular endothelial inflammation remained significant (β = 1.71; P = .02). In nested models, CCL20 added value (χ2 = 79.22; P < .001) to a model already incorporating the Psoriasis Area and Severity Index, Framingham risk, high-sensitivity C-reactive protein, Il-17A, and IL-6 (χ2 = 48.18; P < .001) in predicting vascular endothelial inflammation.
Limitations |
Our study was observational and did not allow for causal inference in the relationship between CCL20 and cardiovascular risk.
Conclusion |
We demonstrate that CCL20 expression has a strong association with vascular endothelial inflammation, reflects systemic inflammation, and may serve as a potential biomarker of impaired vascular health in psoriasis.
Le texte complet de cet article est disponible en PDF.Key words : atherosclerosis, biomarkers, cardiovascular disease, endothelial cell, inflammation, psoriasis, vascular health
Abbreviations used : CCL20, IL, PASI
Plan
Drs Elnabawi and Garshick contributed equally to this article. |
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Funding sources: Supported by a National Institutes of Health (NIH, Bethesda, MD) training grant (T32HL098129), NIH Clinical and Translational Science Awards at New York University Awards (New York, NY) (UL1TR001445, KL2TR001446, and TL1TR001447), American Heart Association Career Development Grant (Dallas, TX) (18CDA34080540), and Dermatology Foundation Research Grant to Dr Garshick; and an American Heart Association Career Development Grant (Dallas, TX) (18CDA34110203AHA) and American Society of Hematology grant (18-A0-00-1001884) to Dr Barrett. Dr Scher was supported, in part, by NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases R01AR074500, the Riley Family Foundation, the Beatriz Snyder Foundation, the Rheumatology Research Foundation, and a National Psoriasis Foundation Grant. Dr Berger was supported, in part, by NIH grants R01HL139909, R01HL114978, and R35HL144993. |
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IRB approval status: This study was approved by the NYU IRBU. |
Vol 84 - N° 4
P. 913-920 - avril 2021 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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